eyeful, btb, BTB-IV, longitudinal lacking, misguided
transcription factor - zinc finger - btb domain - regulates axon guidance - promotes axon growth in part by suppressing expression of the actin nucleation factor Spire - expressed in both glia and neurons - regulates cell fate by antagonizing Notch induction in the Drosophila eye
Gene model reviewed during 5.49
Low-frequency RNA-Seq exon junction(s) not annotated.
Annotated transcripts do not represent all possible combinations of alternative exons and/or alternative promoters.
gene_with_trans_spliced_transcript ; SO:0000459
Gene model reviewed during 5.51
Isoform D interacts with JIL-1.
Click to get a list of regulatory features (enhancers, TFBS, etc.) and gene disruptions (point mutations, indels, etc.) within or overlapping Dmel\lola using the Feature Mapper tool.
Comment: lola probe I (lola-RF); enriched in dorsal cell layer of embryonic CNS
Comment: reported as dorsal/lateral sensory complexes
lola is expressed in all neurons adjacent to the antennal lobe at all developmental stages of development from larva to adult.
Multiple isoforms ofthe lola protein are detected throughout development. In late embryos up to 15 distinct bands can be detected on western blots using an antibody raised to the core BTB/Poz domain shared by all the predicted isoforms.
lola protein distribution (as determined by an antibody that recognizes both protein forms) is consistent with lola transcript distribution but reveals new information. During gastrulation, the protein appears to turn over at mitosis. It is present at highest concentrations in neurons at stage 13 but is also present at substantial levels in epithelial cells and in sensory organ support cells. Unlike the RNA, lola protein is detected in mesodermal nuclei as late as stage 17. It is observed in somatic muscle and in peritracheal cells.
GBrowse - Visual display of RNA-Seq signalsView Dmel\lola in GBrowse 2
Please Note FlyBase no longer curates genomic clone accessions so this list may not be complete
Please Note This section lists cDNAs and ESTs that fall within the genomic extent of the gene model, which may include cDNAs and ESTs of genes within introns, or of overlapping genes. Please see GBrowse for alignment of the cDNAs and ESTs to the gene model.
For each fully sequenced cDNA the DGRC maintains various forms of the cDNA (e.g tagged or untagged) in several different host vectors for subsequent cloning and expression in Drosophila and Drosophila cell lines.
Source for merge of: lola BcDNA:RH31485
Source for merge of: lola BtbIV
Source for merge of: lola l(2)s3697
Source for merge of: lola CG12052 CG18376
Source for merge of: lola sw59 BEST:LD03274
Source for merge of: lola NEST:bs06a08
Source for merge of: lola CG18378 CG18379 CG18380 CG18381
Source for merge of: lola btb
btb[k09901] shows nervous system defects similar to alleles of lola. It also fails to complement several lola alleles, including lola00642, lola5D2, lolaORC4, lolaORE50, lola4E4 and lolaORE120. Previous papers (FBrf0131381) have shown that btb[k09901] complements other alleles of lola, however, lola alleles are known to show intragenic complementation, which can be explained by the trans-splicing that occurs at the lola locus (FBrf0167601). Thus, overall the available evidence indicates that btb[k09901] is an allele of lola.
Annotations CG18376, CG18381, CG18380, CG18379, CG18378 and CG12052 merged as CG12052 in release 3 of the genome annotation.
Source for merge of lola BtbIV was sequence comparison ( date:000202 ).
Source for merge of lola BcDNA:LD17006 was a shared cDNA ( date:030728 ).
The insertion has consistently been shown to map to 47A--47B by in situ hybridization (FBrf0080145, FBrf0131381), consistent with the location of lola (47A). However, the flanking sequences reported in FBrf0131381 (AF175907 and AF175908) map to 94A. Sequencing of the line by the GDP in 2009 (GSS sequences KS308221 and KS308220, reported in FBrf0230166) places the insertion at 2R:10534369 (minus strand) (genome release 6 coordinates). This is within the lola gene, consistent with the in situ localization data and supporting the hypothesis of FBrf0194763 that l(2)k09901 is a lola allele.
The available evidence therefore suggests that the l(2)k09901 line is an allele of lola. Thus the 'btb, bumper-to-bumper' gene (of which l(2)k09901 is the only allele) has been merged with the lola gene and the btb[k09901] allele has been renamed lola[k09901] in FlyBase (date: 2015.10.22).
There have been conflicting results in the literature regarding the location and allelism of the l(2)k09901 insertion line.
FBrf0194763 hypothesised that the l(2)k09901 insertion line is an allele of lola, based on its failure to complement several alleles of lola. In contrast, FBrf0080145 and FBrf0131381 report complementation between l(2)k09901 and lola alleles. As discussed in FBrf0194763, intragenic complementation between other lola alleles has been seen previously (FBrf0167601) and can be explained by the trans-splicing that occurs at the lola locus (FBrf0167601), thus reconciling these apparently conflicting complementation results.
lola is required to regulate stem cell differentiation in type II neural stem cells in the larval central brain.
RNAi generated by PCR using primers directed to this gene causes a cell growth and viability phenotype when assayed in Kc167 and S2R+ cells.
Identification: as a suppressor of the small eye phenotype caused by overexpression of fng in the eye.
Five EMS induced alleles have been identified in a screen for mutations affecting commissure formation in the CNS of the embryo.
Homozygous germline clones have not been recovered. lola may perform some essential function in the germline during oogenesis.
Identification: Enhancer trap screen designed to discover genes involved in the cellular aspects of defense mechanisms, as well as in melanotic tumor formation processes linked to blood cell disregulation.
lola encodes a transcription factor required for axon growth and guidance in the embryo.
In lola mutant embryos growth cones that normally pioneer longitudinal pathways initially extend but then stall, thereby lacking most longitudinal axon pathways.
Mutations lack longitudinal connectives of embryonic ventral nerve cord.